The kidneys excrete potassium: by the main cells of the distal tubule and the manifold
The excretion of potassium from the blood into the lumen is a two-step process that begins with the uptake of the interstitial into the cell by the injection of sodium-potassium ATPase in the lateral membrane.
The cells at the end of the distal tubule and the collecting tubule that excrete potassium are called the primary cell and make up the majority of epithelial cells in these regions.
The figure shows the basic cellular mechanisms of potassium secretion by primary cells.
Figure. Mechanism of potassium excretion and sodium reabsorption by the distal tubule and the manifold main cells.
The excretion of potassium from the blood into the lumen is a two-step process that begins with the uptake of the interstitial into the cell by the injection of sodium-potassium ATPase in the lateral membrane; This pump moves sodium out of the cell into the interstitial space and at the same time moves potassium to the inside of the cell.
The second step in this process is the passive diffusion of potassium from the inside of the cell into the tubular fluid. The ATPase sodium pump creates a high concentration of intracellular potassium, providing the impetus for the passive diffusion of potassium from the cell into the lumen. The main cell membrane has high potency for potassium because there are two special types of channels that allow potassium ions to diffuse rapidly across the membrane: (1) the extracellular potassium channel (ROMK), and (2) the high conductivity Channel Potassium (BK) "large". Both types of potassium channels are required for efficient renal excretion of potassium, and their abundance in cell membranes is increased when more potassium is absorbed.
The main factors that control the potassium excretion of the main cells of the distal tubule and the manifold (1) the action of the sodium pot potassium ATPase pump, (2) the electrochemical gradient for potassium excretion from the blood to the lumen, and (3) membrane permeability to potassium. The three factors that determine potassium excretion are in turn regulated by a number of factors. Interstitial cells may re-absorb or secrete potassium. In cases involving severe potassium deficiency, there is the discontinuation of potassium excretion and reabsorption of potassium in the distal tubules and the manifold. This reabsorption occurs through type A interstitial cells; although this reabsorption is not fully understood, one mechanism believed to contribute is the transport of hydro-potassium ATPase located in the cell membrane. This transporter reabsorbs potassium in exchange for hydrogen ions secreted into the lumen and then diffuses through the membrane of the cell into the bloodstream. This transporter is needed to allow potassium reabsorption during extracellular depletion of potassium, but under normal conditions, it plays only a minor role in controlling potassium secretion.
Figure. Type A and type B manifold cells. Type A cells contain hydro-ATPase and hydro potassium-ATPase in the cell membrane and secrete hydrogen ions while reabsorption of bicarbonate and potassium ions under acidosis. In a type B cell, hydro-ATPase and hydro-potassium-ATPase transporters are located in the basal membrane and reabsorb hydrogen ions while secreting bicarbonate and potassium ions during alkalosis.
When there is excess potassium in body fluids, type B cells alternate in distal tubules and manifold actively secrete potassium into the lumen and have the opposite function of type A cells. Potassium is pumped in. The cell alternates type B with a hydro potassium ATPase pump on the basilar membrane, and then it diffuses into the lumen through potassium channels.